Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CARDIO > Cardiac Impulse > Flashcards

Cardiac Impulse Flashcards

1
Q

what type of rhythm does the heart exhibit

A

autorhythmicity (beats in absence of external stimuli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where do cardiac impulses origionate

A

SAN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do cells in the SAN exhibit

A

spontaneous pacemaker potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define pacemaker potential

A

slowly depolarises the membrane to a threshold to generate an action potential
decreased K efflux
funny current: Na and K influx
Transient Ca influx via T-type Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how do action potentials spread

A

cell-to-cell conduction via gap junctions from SAN to AVN where the AP is delayed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the only point of electrical contact between the atria and ventricles

A

AVN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does an electrical impulse spread from the AVN to the ventricles

A

via the bundle of his branches and the purkinje fibres and cell-to-cell conduction in ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

do action potentials in pacemaker cells differ from action potentials in myocytes

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what effect does the sympathetic NS have on the heart

A

POSITIVE CHRONOTROPIC EFFECT = increased HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does the sympathetic NS increase HR

A

increases slope of pacemaker potential and speeds up conduction through the AVN (by decreasing nodal delay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what effect does the parasympathetic NS have on the heart

A

NEGATIVE CHRONOTROPIC EFFECT = decreases HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does the parasympathetic NS decrease HR

A

decreases the slope of pacemaker potential and slows conduction through AVN (increases nodal delay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what dominates the heart rate under resting conditions

A

vagal tone: exerts a continuous influence to slow intrinsic HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is an ECG

A

a record of the depolarisation and repolarisation cycles of cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where is the SAN located

A

upper right atrium beside SVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when the heart is controlled by the SAN what is this called

A

sinus rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what happens during the rising (depolarisation) of an action potential in pacemaker cells

A

Due to activation of long lasting L-type Ca channels resulting in Ca influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what happens during the falling phase (repolarisation) of an action potential in pacemaker cells

A

Inactivation of L-type Ca channels

activation of K channels causing K efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what neurotransmitter is responsible for sympathetic innervation of the heart and what is its receptor

A

noradrenaline

adrenoceptor B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

why does the parasympathetic NS have no effect on myocytes (only affects APs in SAN and AVN)

A

due to no vagal innervation on ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what neurotransmitter is part of the parasympathetic nervous system and what is its receptor

A

acetylcholine

M2 muscarinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what drug can be used to treat bradycardia to speed up HR as It is a competitive inhibitor of acetylcholine

A

Atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what effect does noradrenaline have on pacemaker K efflux

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what effect does noradrenaline have on Na and Ca influx

A

increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what effect does acetylcholine have on pacemaker cell K efflux

A

increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what effect does acetylcholine have on pacemaker cell Ca and Na influx

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the HR of a patient with bradycardia

A

< 60 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the HR of a patient with tachycardia

A

> 100 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what does the P wave represent

A

atrial depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what does the QRS complex represent

A

ventricular depolarisation (masks atrial repolarisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does the T wave represent

A

Ventricular repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what does the PR interval show

A

largely AVN delay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the ST segment

A

ventricular systole

34
Q

what is the TP interval

A

diastole

35
Q

how are AVN cardiac cells specialised to their function

A

small diameter

slow conduction velocity

36
Q

what is the resting membrane potential of cardiac myocytes

A

-90 mV

37
Q

what causes rapid depolarisation of myocytes and what is the new membrane potential when excited

A

fast Na influx
+20 mV
Phase 0

38
Q

how does the action potential graphs differ in ventricular cardiac myocytes to pacemaker cells

A

myocytes have a plateau phase

due to Ca influx through L-type Ca channels

39
Q

what happens during depolarisation of cardiac myocytes

A

inactivation of Ca channels

activation of K channels = K efflux

40
Q

what happens in phase 0 in ventricular myocyte APs

A

fast Na influx
depolarisation
Na channels rapidly deactivated at threshold to allow Na entry

41
Q

what happens in phase 1 in ventricular myocyte APs

A

closure of Na channels and transient K efflux (different channels from K influx channels)

42
Q

what happens in phase 2 in ventricular myocyte APs

A

Plateau: most important
Balances of conductance:
mainly Ca influx balanced by K efflux (Ca trigger Ca from sacroplasmic reticulum to be released)
Ca influx by L-type channels
membrane potential stays slightly +ve for prolonged steady period

43
Q

what happens in phase 3 in ventricular myocyte APs

A

final repolarisation
closure of Ca channels and K efflux
caused by: Ikr, Its, Ik1 (Ik1 = late period of rapid depolarisation, dominant in phase 4)

44
Q

what happens in phase 4 in ventricular myocyte APs

A

resting membrane potential
drivel of K efflux
Na/K ATPase active so conductance doesn’t change inside and outside the cells

45
Q

what cells show a fast ventricular response

A

atrial and ventricular myocytes

46
Q

how do atrial and ventricular APs differ

A

in atrial APs there is no plateau, additional ultra rapid delayed rectifier outward K current Ikur that is absent from ventricular cells initiates final depolarisation more rapidly

47
Q

what drug does Digoxin target

A

Na/K ATPase inhibitor causes depolarisation

48
Q

what causes depolarisation in SAN and AVN

A

calcium dependant channels

no phase 1 and 2

49
Q

what is phase 4 of an AP in the SAN

A

pacemaker potential
increased inward flux of Ca and Na
only depolarisation
funny current: HCN channel

50
Q

what do HCN channels of the funny current conduct

A

Na and K

switches on at positive potentials

51
Q

where does the funny current take effect

A

end of phase 3

52
Q

what are the 3 important conductance channels important in pacemaker potential

A

Ik: outward flux of K
Ical: inward movement of Ca
If: inward movement of Na causing depolarisation in response to hyperpolarisaton causing funny current

53
Q

why is the slop of pacemaker potentials between action potentials so important

A

sets the intervals and sets HR

54
Q

what happens during phase 0 of a SAN AP

A

upstroke
opening of L-type Ca channels
(NOT voltage activated Na channels)

55
Q

what happens during phase 3 of SAN APs

A

gradual repolarisation due to opening of delayed rectifier K channels mediating Ik
K channels active

56
Q

what are action potentials affected by

A 
drugs
hormones
ANS
cardiac disease 
pH blood 
electrolyte abnormalities
57
Q

what happens once noradrenaline has binded and activated B1 adrenoceptor

A

Gs protein a-subunit binds GTP to adenylyl cyclase

58
Q

what effect does the Gs protein have on B1

A

stimulates B1 to increase SAN AP frequency and HR

increased p.p. slope

59
Q

what enhances the pacemaker potential increased slope

A

If and Ical

60
Q

what reduces the threshold for APs

A

sympathetic NS

enhanced by Ical

61
Q

what is a positive inotropic response

A

increased contractility

increased phase 2 of myocyte AP, increased Ca infux

62
Q

for any end diastolic pressure sympathetic stimulation contractility is higher/lower

A

higher

63
Q

define contractility

A

force of cardiac muscle fibre at any differing degree of stretch

64
Q

what is positive dromotropic response

A

increased conduction velocity in AVN by the sympathetic NS debut to enhanced If and Ical

65
Q

the sympathetic NS increases automaticity what does this mean

A

tendency for non-nodal regions to acquire spontaneous activity

66
Q

what is a Positive Lusitropic action

A

decreased duration of systole

increased uptake of Ca in sarcoplasmic retiulum

67
Q

the sympathetic nervous system decreases/increases the activity of the NA/K ATP ase

A

increases

dépolarises cardiac muscle fibres

68
Q

what long term effect does the sympathetic NS have on the heart

A

increases mass of cardiac muscle/cardiac hypertrophy

69
Q

parasymthatics NS only acts on nodal/myocytes

A

nodal cells

70
Q

what action does acetylcholine take when it activates M2

A

Gi protein

a-subunit inhibits adenylyl cyclase reducing cAMP

71
Q

what is the role of the b/gamma subunit dimer when acetylcholine binds to M2

A

opens specific channels: G protein could inward rectifiers (GIRKs) in SAN

72
Q

what happens when GIRKS open

A

K flows out causing hyperpolarisation

73
Q

what channels reduce the negative chronotropic effect

A

If and Ical

Ical reduces AP threshold increase

74
Q

where does the negative inotropic effect occur

A

decreased contractility

in atria only due to decreased in phase 2 of cardiac action potential and decreased Ca entry

75
Q

what is the negative dromotropic effect

A

decreased conduction in AVN
decreased activation on Ca channels and hyperpolarization via opening of GIRK
AV cells become hyperpolariseed

76
Q

what diseases can parasympathetic NS casue

A

arrhythmias in atria

77
Q

what is the role of the vaxsalva manoever

A

activation of aortic baroreceptors to increase parasympathetic activity in the effect of atrial tachycardia/flutter/fibrillation to suppress conduction

78
Q

what is the role of the funny current

A

modulates pacemaker potential by causing a depolarisation current
mediated by channels activating hyperpolarixation and cAMP

79
Q

what channels control the funny current

A

HCN

80
Q

what drug is used to block HCN channels to decrease the pacemaker slope and decrease HR and is given in conditions where the heart isn’t receiving enough oxygen

A

Ivabradine

CARDIO (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions